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Publication : Receptor editing in a transgenic mouse model: site, efficiency, and role in B cell tolerance and antibody diversification.

First Author  Pelanda R Year  1997
Journal  Immunity Volume  7
Issue  6 Pages  765-75
PubMed ID  9430222 Mgi Jnum  J:111431
Mgi Id  MGI:3653984 Doi  10.1016/s1074-7613(00)80395-7
Citation  Pelanda R, et al. (1997) Receptor editing in a transgenic mouse model: site, efficiency, and role in B cell tolerance and antibody diversification. Immunity 7(6):765-75
abstractText  Mice carrying transgenic rearranged V region genes in their IgH and Igkappa loci to encode an autoreactive specificity direct the emerging autoreactive progenitors into a pre-B cell compartment, in which their receptors are edited by secondary Vkappa-Jkappa rearrangements and RS recombination. Editing is an efficient process, because the mutant mice generate normal numbers of B cells. In a similar nonautoreactive transgenic strain, neither a pre-B cell compartment nor receptor editing was seen. Thus, the pre-B cell compartment may have evolved to edit the receptors of autoreactive cells and later been generally exploited for efficient antibody diversification through the invention of the pre-B cell receptor, mimicking an autoreactive antibody to direct the bulk of the progenitors into that compartment.
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